A human metabolic study was conducted to observe the effect of level of protein intake on urinary calcium, calcium absorption and calcium balance in older adults and to further study the mechanisms of protein-induced hypercalciuria. An increase in protein intake from about 47 to 112 g while maintaining calcium, magnesium and phosphorus intakes constant caused an increase in urinary calcium and a decrease in calcium retention. Glomerular filtration rate was increased and fractional renal tubular reabsorption was decreased by the increase in protein intake; total renal acid, ammonium and sulfate excretions more than doubled, whereas urinary sodium decreased by 38%. The changes in urinary calcium were positively correlated with the increase in total renal acid and sulfate excretion as well as with the decrease in fractional renal tubular reabsorption of calcium. Thus, the data indicate that protein-induced hypercalciuria is due to an increase in glomerular filtration rate and a decrease in fractional renal tubular reabsorption of calcium, the latter of which may be caused by the increased acid load on the renal tubular cells.
Eight young adult males were subjects in a 51-day metabolic study conducted to examine the effects of level of protein and of phosphorus intake on urinary calcium and calcium balance. Two levels of protein (50-150 g) were given at each of two levels of phosphorus intake (1,010 and 2,525 mg). Dietary calcium and magnesium were maintained at 500 and 350 mg, respectively. Raising the protein intake from 50 to 150 g caused a calciuresis at both phosphorus intakes, but the actual increase in urinary calcium was 71 mg/day greater at the low than at the high phosphorus intake and calcium balance was changed from 24 to -116 mg/day at the low phosphorus intake and from 8 to -25 mg/day at the high. When the phosphorus intake was raised, urinary calcium decreased from 156 to 93 mg/day at the low protein intake and from 334 to 200 mg/day at the high protein intake and the markedly negative calcium balance found at the high protein intake was greatly improved. Simultaneous increases in protein and phosphorus intakes caused a 28% increase in urinary calcium whereas the increase in protein intake alone caused a 115% increase.
BackgroundSkeletal muscle loss accompanying aging or cancer is associated with reduced physical function and predicts morbidity and mortality. 3-Methylhistidine (3MH) has been proposed as a biomarker of myofibrillar proteolysis, which may contribute to skeletal muscle loss.MethodsWe hypothesized that the terminal portion of the isotope decay curve following an oral dose of isotopically labeled 3MH can be measured non-invasively from timed spot urine samples. We investigated the feasibility of this approach by determining isotope enrichment in spot urine samples and corresponding plasma samples and whether meat intake up to the time of dosing influences the isotope decay.ResultsIsotope decay constants (k) were similar in plasma and urine, regardless of diet. Post hoc comparison of hourly sampling over 10 h with three samples distributed over 10 or fewer hours suggests that three distributed samples over 5–6 h of plasma or urine sampling yield decay constants similar to those obtained over 10 h of hourly sampling.ConclusionThe findings from this study suggest that an index of 3MH production can be obtained from an easily administered test involving oral administration of a stable isotope tracer of 3MH followed by three plasma or urine samples collected over 5–6 h the next day.
Two 51-day human studies were conducted to investigate the effects of level of protein and phosphorus intake on the various components of renal acid excretion and on urinary sulfate, cyclic AMP and hydroxyproline; the role of the sulfur amino acids (Saa) of the protein was also evaluated. Dietary treatments included: 1) a 50 g protein diet; 2) a 150 g protein diet; and 3) a 50 g protein diet plus Saa to equal that of the 150 g protein diet, each given at 2 levels of phosphorus (1010 and 2525 mg). Calcium intake was 500 mg. Subjects were 16 young adult males. The results are discussed in relationship to calcium data previously reported (1, 2). Changes in renal acid and calcium excretion are not directly related for these reasons: a) the Saa accounted for all of the protein-induced increase in urinary sulfate and acid but for only 43% of the increase in urinary calcium and b) the acid phosphate supplement decreased urinary calcium but increased total acid excretion. The phosphorus supplement increased cyclic AMP but not hydroxyproline excretion. In fact, protein and Saa caused increases in hydroxyproline that were greatly reduced by the phosphorus supplement. Increases in urinary hydroxyproline and calcium were well correlated indicating that, at low calcium intakes, protein or Saa-induced increases in urinary calcium result in increased bone resorption which is reduced by the administration of phosphorus.
The effects on calcium and phosphorus metabolism of adult man by adding meat or meat plus dairy products to a diet low in protein (55 g), calcium (590 mg), and phosphorus (890 mg) were determined. When the low protein diet was consumed, the subjects retained a mean of 20 mg calcium daily but lost 106 mg phosphorus. The addition of meat which increased protein and phosphorus to 146 g and 1660 mg, respectively, caused calcium retention to decrease from 19 to -17 mg but phosphorus retention to increase from 106 to 55 mg. When the meat plus dairy diet high in protein (146 g), calcium (1370 mg), and phosphorus (2060 mg) was consumed the subjects retained substantial amounts of calcium (101 mg) and phosphorus (177 mg). The simulated diets high in purified proteins and supplemented with calcium and phosphorus affected calcium retention in a manner similar to the meat and meat plus dairy diets, but they had a marked negative effect on phosphorus retention; this indicates that supplements of calcium gluconate were well utilized but that those of monopotassium phosphate were not. The results obtained on urinary sulfate, acid, cyclic AMP and hydroxyproline support the conclusions made from the calcium and phosphorus data.
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